Colorectal cancers are one of the most frequent cancers in the United States, with an expected number of 131,200 new cases in 1997. The incidence of colorectal cancers in males and in females has been increasing steadily over the past few decades, while survival rates have shown little improvement. These data indicate that this type of tumors pose a major public health problem. The development of the majority of colorectal cancers occurs via the POLYP-CANCER SEQUENCE . Therefore, at least in theory, preventing the development of the occurrence/ recurrence of neoplastic polyps would result in prevention of colorectal carcinoma. Recent animal experimental and epidemiologic studies in humans have indicated that the incidence of colorectal cancer is inversely related to the consumption of CALCIUM, and to the use of NON- STEROID ANTI-INFLAMMATORY DRUGS (NSAIDs). Both these drugs have been suggested as chemopreventive agents for colorectal cancer. The principal hypothesis to be tested in this study is Calcium supplementation in a dosage of 2,000 mg/day and/or intervention with Piroxicam (7.5 mg/day) reduce the occurrence/recurrence of neoplastic polyps in the colorectum in patients with a recent history of these neoplasms . The study design for the proposed study is a prospective, randomized, double blind, placebo controlled, multicenter clinical trial using a 2 x 2 factorial design. One group of patients will receive 2,000 mg elemental Calcium/day, one will receive 7.5 mg piroxicam/day, one will receive both calcium and piroxicam and one group will receive placebo. The total number of patients required for each group in order to be able to answer the research question is 245 for a total study population of 980. The case-ascertainment period, based on the prevalence of polypectomies in the participating institutions is expected to be 2 years. All study participants will be treated for a period of three years, after which the effect of treatment will be evaluated through a colonoscopy. The apoptotic (Tunel technique) and mitotic (H&E) indices, KI67, COX-2, as well as APC gene, and K-ras mutations (immunohistochemistry) will be measured as surrogate endpoint markers.